Reasearcher BioWhile the etiology of schizophrenia remains elusive, hypofunction of glutamatergic NMDA receptors (NMDAR) is a prime hypothesis. This hypothesis is based mainly on the psychotomimetic action of NMDAR antagonists in healthy subjects. However, when and in which cell-types NMDAR hypofunction takes place, as well as the down-stream effects of this hypofunction are largely unknown. In my laboratory, we employ a multi-disciplinary approach, including immunocytochemistry, slice physiology, in vivo physiology (multi-electrode recording and in vivo microdialysis) and mouse behavioral testing. My recent work has involved the generation of a novel Cre mouse line that allows for selective postnatal genetic manipulations of cortical GABAergic interneurons. Using this Cre line, a transgenic mouse line lacking GluN1 (NR1), an indispensable subunit of NMDARs, in cortical and hippocampal interneurons have provided the first strong evidence that NMDAR hypofunction occurs in cortical GABAergic interneurons during early postnatal development (Nature Neuroscience, 2010).